1. Given the pt’s history and physical exam list your differential diagnosis including at least 5 possible diagnoses. (Remember the differential diagnosis should be broad and really just include causes that could account for the relevant symptoms) Essentially what could account for acute onset dyspnea, chest pain, and tachypnea

Differential diagnoses; Pulmonary embolism, Pneumonia, Pneumothorax, Angina pectoris, Myocardial infarction, cocaine toxicity, Phosgene poisoning

2. Now given the clinical presentation, physical exam and labs What is your top diagnosis? (Use your differential and think through what data lead you to believe your top diagnosis is correct and go against the others)

Troponin levels and the normal EKG rule out Myocardial Infarction

The quality of the pain the lack of radiation suggest against angina

The Xray rules out pnuemothorax

Acute onset suggests against Pneumonia, Near normal WBC, and Xray data exclude pneumonia

Toxin ingestion excluded by denial of ingestion of intoxicants and absence of neurological symptoms and gastrointestinal symptoms. 

The risk factors of hyperlipidemia, history of venous thrombosis, prolonged inactivity associated with air travel, and use of birth control pills are all risk factors for embolus.(Douma 2010)

D-Dimer is a marker of fibrin degradation of a blood clot. It is elevated in cases such as disseminated intravascular coagulation, pulmonary embolism and deep vein thrombosis.  Normal values normal < 250 ng/ml.The D-Dimer test can be falsely positive in cases such as liver disease. However, the patients value of level of >2000ng/ml and other risk factors indicates blood coagulation and supports a diagnosis of PE.  

The “diffuse wheezing in the lower lung fields” suggests fluid in the lungs. . After pulmonary embolism, pressure in the pulmonary artery can double, which increases the rate of fluid effusion into the lung. fluid build up can produce the wheezing observed. 

3. Given your top diagnosis what specific tests do you need to run in order to confirm it?

Symptoms are suggestive of pulmonary embolism. Appropriate diagnostic modalities include CT angiography or ventilation perfusion scintigraphy.(Douma 2010)  I will run a ventilation perfusion scintigraphy (VQ Scan) to assess the ratio of ventilation to perfusion.

a.What is the ventilation perfusion ratio (V/Q ratio)? (Include a short discussion on hypoxic vasoconstriction)

              The Ventilation perfusion ratio (V/Q) is the the ratio between the amount of air getting to the alveoli (the alveolar ventilation, V, in ml/min) and the amount of blood being sent to the lungs (the cardiac output or Q - also in ml/min). In the lungs, areas of lower oxygen (poorly ventilated areas) receive less blood flow. This is Hypoxic vasoconstriction. Hypoxic vasoconstriction serves to shunt blood away from dead spaces and maximize oxygen absorption. In brief, oxygen dependent vasoconstriction prevents blood flow to areas of low oxygen pressure. 

b.What is a V/Q defect? Does a regional V/Q mismatch normally exist in the lungs? What does it tell you? What do you expect for this situation? (Include short discussion of west zones)

              Perfusion increases from the top to the bottom of the lung because of hydrostatic forces. The lung is divided into three west zones with charactersic levels of pressure in the alveolus to the artery. Normally, because of hypoxic vasonconstriction, a well ventilated area is well perfused. A regional V/Q mismatch means that there is a lack of blood flow to a region that is well ventilated. In this situation, there is an embolism and hence, a lack of blood flow to an area. Thus, I expect there to be  a region with uncharacteristically high V/Q ratio (high ventilation/low perfusion) for that region.

c.What is a V/Q scan? How is it performed?

              A V/Q scan measures the ratio of ventilation (air flow) to perfusion (blood flow). This is performed by using inhalation of a radioactive gas to show ventilated areas by visualization of radioactivity. Perfusion is determined by injecting a small amount of radioactive tracer into blood stream.  

d.How would O2 help this patient and how would it change the V/Q ratio?

              Giving oxygen helps increase the oxygenation of the blood and possibly, Increasing the O2 will help dilate the surrounding pulmonary arteries and increase collateral perfusion of the affected area.

e.What is the interpretation of the scan below (Fig 1)? Match this up with the clinical findings.

              There is an area of high ventilation and low perfusion in the left lower quadrant of the lung. This V/Q mismatch suggests a pulmonary embolism in this area. The pulmonary embolism Is located in the left lower quadrant of the left lung which is consistent with the lung sounds heard.

5. Given the positive diagnosis and confirmation of your suspicions what additional tests might be indicated in this patient. Why is that important (Hint: Where did the embolus come from? There was a clinical finding and a major criteria of well’s score that would indicate further testing)

              The emboli most likely came from the leg which is swollen and painful, The wells score as calculated from Medscape  is 7.5 which strongly suggest deep vein thrombosis. To confirm this imaging tests are suggested (Douma 2010) CT angiography or V/Q scans may be used. CT scans result in less radiation to the patient. However, CT scans use iodinated contrast agents These are contraindicated in patients with allergies to tcontrast agents or decreased renal function. The patient has normal creatinine and blood urea levels(Hosten 1990) suggesting normal renal function. 

6. What do we do now that we have the diagnosis? What is the mainstay treatment for a PE? Does this actually remove the clot? There are newer treatment modalities available what is the evidence for these? (Hint: Einstein PE trial)

              The Diagnosis is pulmonary embolism. treatment for PE varies depending upon the character of the presentation and the time from onset.(Van es 2010) Patients who are hemodynamically unstable (massive embolism) are treated with thrombolysis(Van es 2010) 

The mainstay treatment is administration of Heparin followed by long term adminostration of Vitamin K agonists( Van Es 2010) The patient should have been on these pharmacologic agents already. 

The EINSTEIN PE trial says that the mainstay treatment for PE is enoxaparin followed by an adjusted-dose vitamin K antagonist. The mainline treatment is Heparin with concomitant administration of enoxaparin. The NEJM article on the EINSTEIN trial says that Rivaroxaban is comparable to Enoxaparin. The benefit of rivaroxaban is that it requires less inpatient monitoring of the patient.

Sources:

Douma, Renee A., Pieter W. Kamphuisen, and Harry R. Buller. "Acute pulmonary embolism. Part 1: epidemiology and diagnosis." Nature Reviews Cardiology 7.10 (2010): 585+. Academic OneFile. Web. 29 Nov. 2015.

van Es, Josien, et al. "Acute pulmonary embolism. Part 2: treatment." Nature Reviews Cardiology 7.11 (2010): 613+. Academic OneFile. Web. 29 Nov. 2015.


http://www.nejm.org/doi/full/10.1056/NEJMoa1113572

Hosten AO. BUN and Creatinine. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 193.Available from: http://www.ncbi.nlm.nih.gov/books/NBK305/

Guyton and Hall Medical Physiology 2005

Boron and Boulpaep Medical Physiology 2015

http://emedicine.medscape.com/article/300901-workup

https://www.nhlbi.nih.gov/health/health-topics/topics/lvq

http://www.medscape.com/viewarticle/557161

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4078029/pdf/rado-48-02-113.pdf

http://www.nejm.org/doi/full/10.1056/NEJMoa1113572

http://reference.medscape.com/calculator/wells-score-pe